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Influence of the endothelium on the vasorelaxant response to acetylcholine and vasoactive intestinal polypeptide in the isolated rabbit facial artery
Author(s) -
Stojić Dragica,
Radenković Miroslav,
Kršljak Elena,
Popović Jelena,
Pešić Srðan,
Grbović Leposava
Publication year - 2003
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1034/j.1600-0722.2003.00021.x
Subject(s) - vasoactive intestinal peptide , acetylcholine , endocrinology , vasodilation , medicine , phenylephrine , endothelium , adenosine , nitric oxide synthase , cyclooxygenase , forskolin , chemistry , nitric oxide , neuropeptide , stimulation , biochemistry , enzyme , receptor , blood pressure
The aim was to examine the influence of the endothelium on acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) functional responses in the isolated glandular branch of rabbit facial artery precontracted with phenylephrine as well as the potential contribution of nitric oxide (NO) and prostanoids in the ACh‐ and VIP‐induced effects. Acetylcholine caused endothelium‐dependent and VIP endothelium‐independent relaxations of facial artery. The effect of ACh was partly inhibited by N G ‐monomethyl‐ l ‐arginine ( l ‐NMMA, a non‐selective NO synthase inhibitor) or by indomethacin (a cyclooxygenase inhibitor) while being completely blocked after concomitant addition of l ‐NMMA and indomethacin. The relaxation of the facial artery caused by ACh was unaffected by 65 m m KCl. The VIP‐induced vasodilation was potentiated by forskolin (an adenylate cyclase stimulator) and partly reduced by l ‐NMMA or S‐methyl‐ l ‐thiocitrulline ( l ‐SMTC, a neuronal NO synthase inhibitor), whereas it was unaffected by indomethacin. These results suggest that ACh effects on the rabbit facial artery are mediated through release of endothelium‐derived NO and cyclooxygenase products, while the effect of VIP is most probably mediated by an increase of cyclic adenosine 3′,5′‐monophosphate (cAMP) in vascular smooth muscles and by VIP‐induced release of NO from perivascular nerve fibers.